Licoricidin

Licoricidin
Product Name Licoricidin
CAS No.: 30508-27-1
Catalog No.: CFN96389
Molecular Formula: C26H32O5
Molecular Weight: 424.5 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: MMP(e.g.TIMP) | ROS | VEGFR | HIF | NOS | COX | NF-kB | p65 | AP-1
Source: The roots of Glycyrrhiza uralensis.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $388/5mg
Licoricidin, is a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of malignant prostate cancer cells. Licoricidin and licorisoflavan A are effective in inhibiting the growth of all three bacterial species(Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei), with minimal inhibitory concentrations in the range of 2-80 ug /ml, they have a potential for reducing bacterial volatile sulfur compounds (VSCs) production and therefore for controlling halitosis; they also have potential for the development of novel host-modulating strategies for the treatment of cytokine and/or MMP-mediated disorders such as periodontitis. Licoricidin may be considered as an active ingredient in new topically applied anti-ageing formulations, it blocks UVA-induced photoaging via ROS scavenging,this activity converges to limit the activity of MMP-1.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Int J Mol Sci. 2016 Jun 14;17(6). pii: E934
    Licoricidin, an Active Compound in the Hexane/Ethanol Extract of Glycyrrhiza uralensis, Inhibits Lung Metastasis of 4T1 Murine Mammary Carcinoma Cells[Pubmed: 27314329 ]
    Licorice extracts containing glycyrrhizin exhibit anti-carcinogenic properties. Because glycyrrhizin induces severe hypokalemia and hypertension, we prepared a hexane/ethanol extract of Glycyrrhiza uralensis (HEGU) that lacks glycyrrhizin, and showed that HEGU induces apoptosis and G1 cell cycle arrest and inhibits migration of DU145 human prostate cancer cells. Our previous in vitro studies identified two active components in HEGU: isoangustone A, which induces apoptosis and G1 cycle arrest, and Licoricidin, which inhibits metastasis.
    METHODS AND RESULTS:
    This study examined whether HEGU and Licoricidin inhibit metastasis using the 4T1 mammary cancer model. Both HEGU and Licoricidin treatment reduced pulmonary metastasis and the expression of CD45, CD31, HIF-1α, iNOS, COX-2, and VEGF-A in tumor tissues. Additionally, a decrease in protein expression of VEGF-R2, VEGF-C, VEGF-R3, and LYVE-1 was noted in tumor tissues of Licoricidin-treated mice. Furthermore, the blood concentrations of MMP-9, ICAM-1, VCAM-1, and VEGF-A were decreased in HEGU-treated mice. In vitro 4T1 cell culture results showed that both HEGU and Licoricidin inhibited cell migration, MMP-9 secretion, and VCAM expression.
    CONCLUSIONS:
    The present study demonstrates that the Licoricidin in HEGU inhibits lung metastasis of 4T1 mammary carcinoma cells, which may be mediated via inhibition of cancer cell migration, tumor angiogenesis, and lymphangiogenesis.
    Int J Cosmet Sci. 2017 Apr;39(2):133-140.
    Licoricidin, an isoflavonoid isolated from Glycyrrhiza uralensis Fisher, prevents UVA-induced photoaging of human dermal fibroblasts.[Pubmed: 27502959 ]
    Licoricidin is an isoflavonoid isolated from Glycyrrhiza uralensis Fisher. In this study, we investigated the effects of Licoricidin on photoaging of UVA-irradiated human dermal fibroblasts (HDFs).
    METHODS AND RESULTS:
    In vitro reactive oxygen species (ROS) scavenging activity, cellular protective effect and inhibition of elastase activity was determined by Fe3+ -EDTA/H2 O2 systems, photohaemolysis and elastase activity assay, respectively. Anti-oxidative capacity of the compound was evaluated by fluorescent ELISA and 2', 7'-dichlorofluorescin-diacetate (DCF-DA) assay. The expression of protein and phosphorylation was examined using Western blot. The ROS scavenging activity (OSC50 ) of Licoricidin was 2.77 μM. It was 3.1-fold higher than that of L-ascorbic acid. Its protective effects were confirmed in a study of 1 O2 -induced cellular damage to human erythrocytes. The τ50 value of 10 μM of Licoricidin was 71.0 min; this was markedly higher than that obtained with α-tocopherol (37.0 min). The elastase inhibitory activity of Licoricidin (IC50 of 61.2 μM) was 2.1-fold more potent than that of oleanolic acid. Licoricidin markedly reduced the UVA-induced intracellular ROS in a concentration-dependent manner. Western blot revealed that Licoricidin attenuated the UVA-dependent induction of MMP-1 protein. Mechanistically, this appeared to be due to Licoricidin-dependent inhibition of mitogen-activated protein kinases (MAPK) phosphorylation, which resulted in decreased c-Jun activation and reduced c-Jun and c-Fos expression.
    CONCLUSIONS:
    Licoricidin blocks UVA-induced photoaging via ROS scavenging. This activity converges to limit the activity of MMP-1. These data suggest that Licoricidin may be considered as an active ingredient in new topically applied anti-ageing formulations.
    J Breath Res. 2012 Mar;6(1):016006
    Reduction of bacterial volatile sulfur compound production by licoricidin and licorisoflavan A from licorice.[Pubmed: 22368239 ]
    Halitosis affects a large proportion of the population and is, in most cases, caused by the production of volatile sulfur compounds (VSCs), particularly methyl mercaptan and hydrogen sulfide, by specific bacterial species colonizing the oral cavity.
    METHODS AND RESULTS:
    In this study, a supercritical extract of Chinese licorice (Glycyrrhiza uralensis), and its major isoflavans, Licoricidin and licorisoflavan A, were investigated for their effect on growth, VSC production and protease activity of Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei, which have been associated with halitosis. The effects of licorice extract, Licoricidin, and licorisoflavan A on VSC production in a saliva model were also tested. We first showed that Licoricidin and licorisoflavan A, and to a lesser extent the licorice extract, were effective in inhibiting the growth of all three bacterial species, with minimal inhibitory concentrations in the range of 2-80 μg ml(-1).
    CONCLUSIONS:
    Within the limitations of this study, it can be concluded that a licorice supercritical extract and its major isoflavans (Licoricidin and licorisoflavan A) represent natural ingredients with a potential for reducing bacterial VSC production and therefore for controlling halitosis.
    Br J Nutr. 2010 Nov;104(9):1272-82
    Hexane-ethanol extract of Glycyrrhiza uralensis containing licoricidin inhibits the metastatic capacity of DU145 human prostate cancer cells.[Pubmed: 20487583 ]
    Licorice extracts are known to exhibit anti-carcinogenic activities. However, chronic licorice consumption can lead to serious side effects due to the presence of considerable quantities of glycyrrhizin, which causes severe hypokalaemia and hypertension.
    METHODS AND RESULTS:
    In the present study, we evaluated the effects of a hexane-ethanol extract of Glycyrrhiza uralensis (HEGU), which lacks glycyrrhizin, on the metastatic characteristics of DU145 prostate cancer cells. HEGU inhibited basal and epidermal growth factor-induced cell migration, invasion and adhesion in a dose-dependent fashion. HEGU significantly suppressed the secretion and activation of the matrix metalloproteinase (MMP)-2 and MMP-9. The secretion of tissue inhibitor of metalloproteinase (TIMP)-1 was reduced, but that of TIMP-2 was increased in HEGU-treated cells. HEGU reduced the protein levels of integrin-α2, the intercellular adhesion molecule, and the vascular cell adhesion molecule. An active fraction of HEGU was separated via column chromatography, and the structure of the active component, Licoricidin, was identified via 1H NMR and 13C NMR. The treatment of DU145 cells with Licoricidin induced a reduction in cell migration and the secretion of MMP-9, TIMP-1, urokinase-type plasminogen activator and vascular endothelial growth factor, as well as in the expression of adhesion molecules.
    CONCLUSIONS:
    These results indicate that HEGU, which contains Licoricidin, is a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of malignant prostate cancer cells. The observed reductions in the activation of proteases and the levels of adhesion molecules may constitute a component of the mechanisms by which HEGU inhibits the migration and adhesion of prostate cancer cells.
    J Periodontol. 2011 Jan;82(1):122-8.
    Modulation of matrix metalloproteinase and cytokine production by licorice isolates licoricidin and licorisoflavan A: potential therapeutic approach for periodontitis[Pubmed: 20722535]
    Inflammatory cytokines and matrix metalloproteinases (MMPs) produced by resident and inflammatory cells in response to periodontopathogens play a major role in the tissue destruction observed in periodontitis, which is a disease that affects tooth-supporting structures. In the present study, we investigate the effects of licorice-derived Licoricidin (LC) and licorisoflavan A (LIA) on the secretion of various cytokines and MMPs by human monocyte-derived macrophages stimulated with Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) lipopolysaccharide (LPS).
    METHODS AND RESULTS:
    Macrophages were treated with non-toxic concentrations of LC or LIA before being stimulated with A. actinomycetemcomitans LPS. The secretion of cytokines and MMPs and the activation of nuclear factor-kappa B (NF-κB) p65 and activator protein (AP)-1 were assessed by enzyme-linked immunosorbent assays. LC and LIA inhibited the secretion of interleukin (IL)-6 and chemokine (C-C motif) ligand 5 in a concentration-dependent manner but did not affect the secretion of IL-8 by LPS-stimulated macrophages. LC and LIA also inhibited the secretion of MMP-7, -8, and -9 by macrophages. The suppression of cytokine and MMP secretion by LC and LIA was associated with the reduced activation of NF-κB p65 but not that of AP-1.
    CONCLUSIONS:
    The present study suggests that LC and LIA have potential for the development of novel host-modulating strategies for the treatment of cytokine and/or MMP-mediated disorders such as periodontitis.
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